Imitation often occurs automatically and unconsciously, especially during social interactions. Imitation is thought to rely on a specialized neural system that contains neurons responsive to both action observation and action execution. These so-called mirror neurons provide a parsimonious mechanism to translate visual information about an action into the motor representation necessary to produce the same action, by specifically modulating the excitability of the primary motor representation of the action. This model is able to explain the automatic tendency to imitate, however it is not clear how this automatic tendency is controlled to prevent perpetual imitation. The goal of the current proposal is to elucidate the neural mechanisms that control the automatic tendency to imitate. In light of neurological and psychiatric patients with imitation control deficits, as well as early research suggesting a distinct inhibitory mechanism for control imitation, we predict that control of imitation occurs through a specialized control network and that it may involve modulation of the mirror neuron system. Impaired imitation is a hallmark of autism spectrum disorders. Due to the proposed role of mirror neurons in understanding others' actions and emotions, recent research has examined mirror neuron function in autism. Converging evidence suggests that activity in the human mirror neuron system may be decreased in autism spectrum disorders compared to typically developing children. However, the etiology of this decrease in activity has not been explored. Two possibilities include intrinsic mirror neuron system dysfunction and impaired regulation of the mirror neuron system by distinct neural circuitry. Understanding control of imitation in typical subjects will pave the way for studies in autism that can disentangle these two possibilities as well as provide insight into the neural underpinnings of the imitative deficits. In Aim 1, two functional magnetic resonance imaging studies are planned to compare inhibition of imitation directly with better understood inhibitory mechanisms. Control of imitation will be compared with response inhibition, as measured by the stop-signal paradigm. In addition, imitation control and resolution of interference in a spatial compatibility task will be compared, since interference resolution has been argued to rely on distinct cognitive control processes. In Aim 2, transcranial magnetic stimulation will be used to evaluate the causal roles of commonly studied control mechanisms in control of imitation. Improved understanding of control of imitation at a basic level in normal populations will provide a platform to explore deficits in imitation and the mirror neuron system in psychiatric illnesses such as autism spectrum disorders.